More surprises in the global greenhouse: Human health impacts from recent toxic marine aerosol formations, due to centennial alterations of world-wide coastal food webs.

Reductions of zooplankton biomasses and grazing pressures were observed during overfishing-induced trophic cascades and concurrent oil spills at global scales. Recent phytoplankton increments followed, once Fe-, P-, and N-nutrient limitations of commensal diazotrophs and dinoflagellates were also eliminated by respective human desertification, deforestation, and eutrophication during climate changes. Si-limitation of diatoms instead ensued during these last anthropogenic perturbations of agricultural effluents and sewage loadings. Consequently, ~15% of total world-wide annual asthma trigger responses, i.e. amounting to ~45 million adjacent humans during 2004, resulted from brevetoxin and palytoxin poisons in aerosol forms of western boundary current origins. They were denoted by greater global harmful algal bloom [HAB] abundances and breathing attacks among sea-side children during prior decadal surveys of asthma prevalence, compiled here in ten paired shelf ecosystems of western and eutrophied boundary currents. Since 1965, such inferred onshore fluxes of aerosolized DOC poisons of HABs may have served as additional wind-borne organic carriers of toxic marine MeHg, phthalate, and DDT/DDE vectors, traced by radio-iodine isotopes to potentially elicit carcinomas. During these exchanges, as much as 40% of mercury poisonings may instead have been effected by inhalation of collateral HAB-carried marine neurotoxic aerosols of MeHg, not just from eating marine fish. Health impacts in some areas were additional asthma and pneumonia episodes, as well as endocrine disruptions among the same adjacent humans, with known large local rates of thyroid cancers, physician-diagnosed pulmonary problems, and ubiquitous high indices of mercury in hair, pesticides in breast milk, and phthalates in urine.

Red tides in the Gulf of Mexico: Where, when, and why?

[1] Independent data from the Gulf of Mexico are used to develop and test the hypothesis that the same sequence of physical and ecological events each year allows the toxic dinoflagellate Karenia brevis to become dominant. A phosphorus-rich nutrient supply initiates phytoplankton succession, once deposition events of Saharan iron-rich dust allow Trichodesmium blooms to utilize ubiquitous dissolved nitrogen gas within otherwise nitrogen-poor sea water. They and the co-occurring K. brevis are positioned within the bottom Ekman layers, as a consequence of their similar diel vertical migration patterns on the middle shelf. Upon onshore upwelling of these near-bottom seed populations to CDOM-rich surface waters of coastal regions, light-inhibition of the small red tide of ~1 ug chl l(-1) of ichthytoxic K. brevis is alleviated. Thence, dead fish serve as a supplementary nutrient source, yielding large, self-shaded red tides of ~10 ug chl l(-1). The source of phosphorus is mainly of fossil origin off west Florida, where past nutrient additions from the eutrophied Lake Okeechobee had minimal impact. In contrast, the P-sources are of mainly anthropogenic origin off Texas, since both the nutrient loadings of Mississippi River and the spatial extent of the downstream red tides have increased over the last 100 years. During the past century and particularly within the last decade, previously cryptic Karenia spp. have caused toxic red tides in similar coastal habitats of other western boundary currents off Japan, China, New Zealand, Australia, and South Africa, downstream of the Gobi, Simpson, Great Western, and Kalahari Deserts, in a global response to both desertification and eutrophication.